1. Field of the Invention
The present invention relates to a composition for preventing or treating cervical cancer comprising a human papillomavirus (HPV) plasmodium and an immunity enhancer, and, more particularly, to a fusion protein including a fusion polypeptide recombined to transform a 3-dimensional (3D) structure of E6 and E7, which are antigens of types 16 and 18 HPV, a signal peptide for secreting the fusion polypeptide outside the cells, and an immunity enhancer peptide present in an individual, wherein the fusion protein may treat HPV-triggered tumors by inducing an immune response specific to HPV type 16 and 18 antigens.
Incorporated by reference herein in its entirety is the Sequence Listing entitled “PCT_KR2010—005367_Sequence Listing_ST25-2,” created Apr. 4, 2014, size of 11 kilobytes.
2. Discussion of Related Art
Cervical cancer has been known as a disease that develops from infection of human papillomaviruses (HPVs) of very high concern such as types 16 and 18 (zur Hausen, H et al. Biochem Biophys Acta 1996, 1288; F55-F78, Mark H et al. J Natl Cancer Inst 1993, 85; 958-964). Among HPV proteins, E6 and E7 proteins play an important role in the onset of cervical cancer, and are important target substances used to prepare a vaccine for treating and preventing cervical cancer since they are confirmed to be expressed in 99% of tumor tissues from cervical cancer patients (von Knebel Doeberitz et al. Int. J. Cancer 1992, 51; 831-834). In this case, E6 is bound to p53 known as a tumor suppressor protein to facilitate degradation of the p53, thereby obstructing a cell cycle from leading to the apoptosis pathway, and E7 is bound to a retinoblastoma protein, pRb, known as a tumor suppressor factor to inactivate the retinoblastoma protein and facilitate degradation of the retinoblastoma protein, thereby allowing the cell cycle to enter the S stage (Cobrinik et al., Trends Biochem Sci 1992, 17:312-5).
In clinical trials using a composition including a nucleic acid sequence in which HPV16 E6 and E7 proteins are simultaneously expressed to treat cervical cancer, however, the composition has shown a poor therapeutic effect (Garcia F et al. Obstet Gynecol 2004, 103; 317-326). These results indicate that a sufficient antigen-specific immune response to treat or suppress cervical cancer is not triggered when only an HPV antigen is simply administered.
Therefore, it is necessary to enhance the immunogenicity of E6 and E7 proteins to treat cervical cancer, and remove the proteins' capability of developing into cancer.